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RNA resequencing of liver in macrophage-specific-Pparg knockout mice model

ABSTRACT: Wild type and macrophage-specific-Pparg knockout C57 mice were gavaged with CMC or DEHP for 28 or 90continuous days. At the end of the experiment, livers were harvested for RNA-seq. Data analysis revealed that DEHP induced remarkable changes of lipid metabolic genes in liver, and that loss of Pparg in hepatic macrophages significantly abrogated the elevation of gene overexpression associated with fatty acid metabolism.

ORGANISM(S): Mus musculus

PROVIDER: GSE160373 | GEO | 2021/04/01

REPOSITORIES: GEO

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RNA resequencing of liver in liver-specific-Pparg knockout mice model

Project description:Two groups of liver-specific-Pparg knockout C57 mice were gavaged with CMC or DEHP for 28 continuous days. At the end of the experiment, livers were harvested for RNA-seq, we found that metabolism related genes were significantly changed by DEHP in paralell with the PPAR signaling pathway.

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Whole genome resequencing of liver in mice model

Project description:Four groups of C57 mice were gavaged with CMC, ethanol, DEHP and ethanol+DEHP for 28 continuous days. At the end of the experiment, livers were harvested to carry out Whole genome resequencing, we found that metabolism related genes were significantly changed in the DEHP and ethanol+DEHP groups compared with control groups, but there was no significant change between them.

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Placental PPARg-Regulated Genes

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Placental PPARg-Regulated Genes

Project description:Robust identification of placental PPARg target genes via mutliple PPARg-dependence criteria. Integration of differential expression data from Pparg-null, Rxra-null, Med1-nul and Ncoa6-null placentas and from WT and Pparg-null Trophoblast stem cells (TSC) differentiated for 2 or 4 days in the presence or absence of the PPARg agonist Rosiglitazone (Rosi). [Placentas] Three pools of three WT placentas, each vs a litter-matched pool of three Pparg-null placentas Three pools of three WT placentas, each vs a litter-matched pool of three Rxra-null placentas Three pools of three WT placentas, each vs a litter-matched pool of three Med1-null placentas Three pools of three WT placentas, each vs a litter-matched pool of three Ncoa6-null placentas [Trophoblast stem cells (TSC)] Three independent WT TSC lines differentiated for two and four days in the presence or absence of Rosi vs two independent Pparg-null TSC lines differntiated for the same durations in the presence of Rosi

2012-07-09 | E-GEOD-39233 | biostudies-arrayexpress

PPARg and IL-4-induced gene expression data from PPARg +/- LysCre and PPARg fl/- LysCre mouse bone marrow-derived macrophages

Project description:Conditional macrophage-specific PPARg knockout mice were generated on C57Bl/6 background by breeding PPARg fl/- (one allele is floxed, the other is null) and lysozyme Cre transgenic mice. PPARg and IL-4 signaling was analyzed on bone marrow-derived macrophages. Bone marrow of 3 mice per group was isolated and differentiated to macrophages with M-CSF (20 ng/ml). 20 ng/ml IL-4 was used to induce alternative macrophage activation and 1 uM Rosiglitazone (RSG) was used to activate PPARg. From each mouse 4 samples were generated: 1. M-CSF, 2. M-CSF+RSG, 3. IL-4 and 4. IL-4+RSG. All compounds were added throughout the whole differentiation process, and fresh media was added every other day. Control cells were treated with vehicle (DMSO:ethanol). After 10 days, RNA was isolated and gene expression profiles were analyzed using Mouse Genome 430 2.0 microarrays from Affymetrix. 3 PPARg +/- LysCre and 3 PPARg fl/- LysCre mice were used to isolate bone marrow and from each macrophages were differentiated with or without IL-4 and simultaneously treated with vehicle or RSG. Altogether we analyzed 24 samples with 3 biological replicates as below.

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PPARG interactions with UBR5 and MRE11-RAD50-NBS1 are required for DNA damage response and repair.

Project description:PPARG interactome datasets containing (1) Flag-PPARG AP-MS, identifying MRE11, RAD50 and NBS1 as novel interactors, (2) tandem-IP (in solution and silver fragments) of PPARG-Strep and Flag-NBS1, which identifies PPARG interaction with UBR5 (3) tandem-IP (same as 2) with BS3 cross-linking illustrates the binding interface between PPARG and NBS1. These mass spec data and other biochemical data demonstrate PPARG novel roles in promoting DNA damage response and repair, by activating the ATM pathway.

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PPARg and IL-4-induced gene expression data from PPARg +/- LysCre and PPARg fl/- LysCre mouse bone marrow-derived macrophages

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PPARg controls proinflammatory responses in alveolar macrophages

Project description:Tissue resident macrophages are a heterogeneous population with unique functions. During steady state conditions most tissue macrophages are of embryonic origin and maintained locally. Despite their common fetal origin, tissue macrophages are able to fulfil tissue specific functions, suggesting that the local environment can modulate cell function. It has been reported that PPARg is critical for the development of macrophages in the lung. Here, we show that PPARg functions as a transcriptional repressor in alveolar macrophages. Alveolar macrophages lacking Pparg responded more strongly to LPS stimulation by producing more cytokines and phagocytosed more particles in vitro. Certain prostaglandins can act as endogenous ligands for PPARg. We show that prostaglandins were expressed in an organ-specific fashion and modulated cytokine production by alveolar macrophages as well as bone marrow-derived macrophages and monocytic U937 cells. Pparg expression was further induced in macrophages by different cytokine combinations including IL-4, IL-3 and IL-13 suggesting a global role for PPARg which can be regulated by the local environment on two levels. Lastly, repression of inflammatory genes was mediated by PPARg interacting with NFkB and STAT signalling cascades rather than direct transrepression. Therefore PPARg is a modulator of macrophage functions, that changes the inflammatory state of macrophages by regulating classical immune signalling cascades.

2018-03-01 | GSE103102 | GEO

PPARg and IL-4-induced gene expression data from PPARg +/- LysCre and PPARg fl/- LysCre mouse bone marrow-derived alternatively activated macrophages and immature dendritic cells (iDCs)

Project description:Conditional macrophage-specific PPARg knockout mice were generated on C57Bl/6 background by breeding PPARg fl/- (one allele is floxed, the other is null) and lysozyme Cre transgenic mice. PPARg and IL-4 signaling was analyzed on bone marrow-derived macrophages. Bone marrow of 4 mice per group was isolated and differentiated to alternatively activated macrophages with 20 ng/ml M-CSF and 20 ng/ml IL-4 or to iDCs with 20 ng/ml GM-CSF+20 ng/ml IL-4. 1 uM Rosiglitazone (RSG) was used to activate PPARg. From each mouse 4 samples were generated: 1. M-CSF+IL-4, 2. M-CSF+IL-4+RSG, 3. GM-CSF+IL-4 and 4. GM-CSF+IL-4+RSG. All compounds were added throughout the whole differentiation process, and fresh media was added every other day. Control cells were treated with vehicle (DMSO:ethanol). After 9 days, RNA was isolated and gene expression profiles were analyzed using ABI Mouse Genome Survey Arrays. 4 PPARg +/- LysCre and 4 PPARg fl/- LysCre mice were used to isolate bone marrow and from each alternatively activated macrophages were differentiated with IL-4 and simultaneously treated with vehicle or RSG, iDCs were differentiated with GM-CSF+IL-4 and simultaneously treated with vehicle or RSG. Altogether we analyzed 32 samples with 4 biological replicates as below.

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